Pathophysiology of the arterial wall. Purpose of this work is to study certain aspects of the structure and function of the arterial wall that are - or may be - related to atherosclerosis. (1) Endothelial contraction in large arteries. It has been stated recently that endothelial contraction is the initial step in the atherosclerotic lesion, by causing leakage of blood-borne material into the wall. Agents such as angiotensin II and bradykinin were said to induce such contraction, hence the current treatment of atherosclerosis with "cell relaxants". We plan to verify this concept in the rat. Vasoactive agents will be tested by perfusion through the aorta or by injection into the intact arterial system. The arterial wall will then be studied by electron microscopy; markers will help to uncover any leakage into the arterial wall (Evans blue at the gross level; carbon black, ferritin, etc., at the EM level). (2) "Granulovesicular Material". The arteries of adult animals develop deposits of "granulovesicular material" of unclear origin (possibly fragmentation of death of smooth muscle cells). We will study this material by EM, in the coronary artery of the rat (pathogenesis, relation aging, to atherosclerosis, to arterial involution as seen in the post-partum uterine artery). (3) Phagocytosis within the arterial wall. Various organic and inert materials will be injected into the wall of large arteries in the dog or pig, and their disposal will be studied by light and electron microscopy. Cellular changes in myocardial infarction. We have recently found a myocardial change that develops almost immediately after myocardial infarction (in the rat, by 5 minutes): the fibers become stretched and wavy. We plan to produce reversible myocardial infarction in the pig or dog, and study primarily the "wavy fibers" under various angles (EM; histochemistry; reversibility).